The objective of the study is to analyze in detail biochemical and pathophysiological factors that are responsible for causing neuronal damage in the brain in conditions of ischemia, hypoxia, hypoglycemia and status epilepticus. The pathological conditions under study are reproduced in animal experiments under control of physiological variables, including cerebral blood flow and rates of utilization of oxygen and glucose. Changes in cerebral energy metabolism are evaluated from measurements of tissue concentrations of labile organic phosphates, glycolytic metabolites, citric acid cycle intermediates, associated amino acids, and ammonia. Cellular damage is assessed by histopathological examination. Considerable emphasis is laid on prophylactic and therapeutic measures that can minimize or prevent energy failure at cellular level or on conditions that aggravate the effect of energy deficit on revival of function, metabolism or cell structure.